Coptisine Prevented IL-β-Induced Expression of Inflammatory Mediators in Chondrocytes

Abstract

Interleukin 1β (IL-1β) is a pleiotropic pro-inflammatory cytokine that plays a critical role in the development of osteoarthritis (OA). Coptisine is an isoquinoline alkaloid extracted from Coptidis rhizome and has been reported to possess anti-inflammatory activity. However, the anti-inflammatory effects of coptisine on interleukin-1 beta (IL-1β)-stimulated chondrocytes have not been reported. Therefore, the aim of this study was to investigate the effects of coptisine on IL-1β-induced inflammation in human articular chondrocytes. Our results showed that coptisine greatly inhibited the production of nitric oxide (NO) and prostaglandin E2 (PGE2), as well as suppressed the expression of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) in human OA chondrocytes induced by IL-1β. It also inhibited the expression of matrix metalloproteinase-3 (MMP-3) and MMP-13 in IL-1β-stimulated human OA chondrocytes. Furthermore, coptisine significantly inhibited the IL-1β-induced NF-kB activation in human OA chondrocytes. Taken together, these data suggest that coptisine inhibits the IL-1β-induced inflammatory response by suppressing the NF-kB signaling pathway. Thus, coptisine may be a potential agent in the treatment of OA.

Betulin suppressed interleukin-1β-induced gene expression, secretion and proteolytic activity of matrix metalloproteinase in cultured articular chondrocytes and production of matrix metalloproteinase in the knee joint of rat

“…According to several reports, IL-1β-stimulated expression of MMPs is associated with the suppression of the NF-κB signaling pathway [36373839]. Jung and his colleagues reported that Schisandrae Fructus, an anti-inflammatory medicinal plant used in folk medicine, inhibited IL-1β-induced expression and activity of MMP-1, MMP-3, and MMP-13 and markedly suppressed the nuclear translocation of NF-κB by blocking IkB-alpha degradation in SW1353 human chondrocytes [36].…”

“…Another natural product, matrine, inhibited IL-1β-induced expression of MMPs by suppressing the activation NF-κB in human chondrocytes in vitro [38]. Zhou et al reported that coptisine, an isoquinoline alkaloid extracted from an antiinflammatory medicinal plant, also inhibited the expression of MMP-3 and MMP-13 through inhibition of NF-κB activation in human chondrocytes [39]. …”

Effect of oleanolic acid on the activity, secretion and gene expression of matrix metalloproteinase-3 in articular chondrocytesin vitroand the production of matrix metalloproteinase-3in vivo

“…As claimed by several reports, IL-1β-stimulated expression of MMPs is associated with the suppression of the NF-κB signaling pathway [36373839]. It was reported that coptisine, an isoquinoline alkaloid extracted from an anti-inflammatory medicinal plant, also inhibited the expression of MMP-3 and MMP-13 through inhibition of NF-κB activation in human chondrocytes [36].…”

“…It was reported that coptisine, an isoquinoline alkaloid extracted from an anti-inflammatory medicinal plant, also inhibited the expression of MMP-3 and MMP-13 through inhibition of NF-κB activation in human chondrocytes [36]. Another natural product, matrine, inhibited IL-1β-induced expression of MMPs by suppressing the activation NF-κB in human chondrocytes in vitro [37].…”

The herbal decoction modified Danggui Buxue Tang attenuates immune-mediated bone marrow failure by regulating the differentiation of T lymphocytes in an immune-induced aplastic anemia mouse model

“…Pharmacological study confirmed that magnoflorine could regulate the differentiation of neutrophils and T cells for anti-inflammation [45]. Coptisine and calycosin could modulate the activation of the nuclear factor-κB (NF-κB), MAPK or PI3K/Akt/GSK-3 signaling pathways, contributing to an inhibitory effect on the inflammatory response induced by pro-inflammatory cytokines [46, 47]. Jatrorrhizine [47], berberine [48] and palmatine [49] have inhibitory functions on cell apoptosis through anti-oxidative activation or intervening in the inducible nitric monoxide synthase system.…”